Clinical analysis of the serum muscle enzyme spectrum of patients with newly diagnosed Sheehan's syndrome.

We investigated the factors associated with serum muscle enzyme elevation in patients with Sheehan's syndrome. A total of 48 patients who were newly diagnosed with Sheehan's syndrome were included and divided into 3 groups: Group 1, creatine kinase (CK) ≥ 1000 U/L; Group 2, 140 < CK < 1000 U/L; and Group 3, CK ≤ 140 U/L. Differences in serum muscle enzymes, serum electrolytes, blood glucose and hormones were compared among the 3 groups. A Spearman correlation analysis and multiple linear regression analysis were performed on serum muscle enzymes and the other variables. Four patients in Group 1 underwent electromyography. Fourteen, 26 and 8 patients were divided into Group 1, Group 2, and Group 3, respectively. The levels of plasma osmolality, serum sodium, free triiodothyronine (FT3) and free thyroxine (FT4) in Group 1 were lower than those in Group 3 at admission (P < .05). There were significant differences in CK, CK-MB, aspartate aminotransferase, lactate dehydrogenase, and alpha-hydroxybutyrate dehydrogenase among the three groups (P < .05). CK was correlated with serum sodium (r = -0.642, P < .001), serum potassium (r = -0.29, P = .046), plasma osmolality (r = -0.65, P < .001), FT3 (r = -0.363, P = .012), and FT4 (r = -0.450, P = .002). Moreover, creatine kinase isoenzyme-MB (CK-MB) was correlated with serum sodium (r = -0.464, P = .001) and plasma osmolality (r = -0.483, P < .001). The multiple linear regression showed that serum sodium was independently and negatively correlated with CK (r = -0.352, P = .021). The electromyogram results supported the existence of myogenic injury. Sheehan's syndrome is prone to be complicated by nontraumatic rhabdomyolysis, with both a chronic course and acute exacerbation. Serum muscle enzymes should be routinely measured. For patients with CK levels > 1000 U/L, a CK-MB/CK ratio < 6% can be a simple indicator to differentiate rhabdomyolysis from acute myocardial infarction. Abnormal serum muscle enzymes observed in Sheehan's syndrome may be associated with hypothyroidism and with hyponatremia in particular.

Aldosterone/direct renin concentration ratio as a screening test for primary aldosteronism: a systematic review and meta-analysis.

Background: Primary aldosteronism (PA) refers to a spontaneous increase in adrenal aldosterone secretion, and is considered the main cause of secondary hypertension. The main aldosterone screening methods include plasma aldosterone-to-renin ratio (ARR) and plasma aldosterone/direct renin concentration ratio (ADRR). The ARR method has many limitations such as complex operation, several influencing factors, and difficulty in standardization. Relatively speaking, ADRR has gradually attracted attention due to its simple operation, stable results, and easy standardization. However, different research results have suggested that the diagnostic efficacy of ADRR in the screening of primary aldosteronism varies greatly. Meta-analysis may be a way to provide evidence-based medicine. Therefore, it is necessary to conduct a meta-analysis of the diagnostic efficacy of ADRR in primary aldosteronism to clarify the role of ADRR in the screening of PA. Methods: The words "primary aldosteronism", "primary hyperaldosteronism", "aldosterone", "renin concentration", "hypertension" and "screening test" were used as search terms. Literature searches were conducted in the databases of PubMed, Embase, Cochrane Library, and China National Knowledge Infrastructure (CNKI), Wanfang, and Weipu. According to the PICOS principles studies exploring the effectiveness of ADRR in screening for PA were included in the analysis. The research data were independently extracted and analyzed by 2 researchers. Quality assessment of diagnostic accuracy studies (QUADAS-2) was used to analyze the risk bias of the included studies. Results: The results showed that 10 studies met the inclusion criteria, with a total of 2,806 subjects. The meta-analysis found that the overall sensitivity and specificity were 0.87 [95% confidence interval (CI): 0.85-0.89], 0.85 (95% CI: 0.83-0.86), respectively. The area under the curve (AUC) of the summary receiver operating characteristic (SROC) curve was 0.9333. The pooled positive likelihood ratio (PLR), pooled negative likelihood ratio (NLR), and pooled diagnostic odds ratio (DOR) were 5.84 (3.67-9.30), 0.16 (0.12-0.22), and 39.82 (22.84-69.44), respectively. Discussion: This study confirmed that ADRR screening for PA has good sensitivity and specificity. Therefore, ADRR can be used to screen for PA. But the risk and problematic control should be considered.

Functional importance of the TGF-ß1/Smad3 signaling pathway in oxygen-glucose-deprived (OGD) microglia and rats with cerebral ischemia.

We investigated the transforming growth factor-b1 (TGF-ß1)/Smad3 signaling pathway in rats with cerebral ischemia and oxygen-glucose-deprived (OGD) microglia. Cerebral ischemia is a clinical condition that occurs when insufficient blood flows to the brain to maintain metabolic activity. TGF-ß1 is a well-known functional peptide that regulates cell differentiation, migration, proliferation, and apoptosis. In the current study, we determined the infarct size and TGF-ß1/Smad3 protein expression in stroke-induced rats. Apoptosis and TGF-ß1/Smad3 mRNA and protein expression were determined in transfected OGD human microglial cells. TGF-ß1 treatment resulted in smaller infarct regions than in control cells, whereas TGF-ß1 inhibitor treatment resulted in larger infarcts. The TGF-ß1-treated groups showed substantial TGF-ß1 and Smad3 expression by immunofluorescence compared to the controls. Apoptosis was significantly reduced in TGF-ß1- and Smad3-transfected cells, and an increased rate of apoptosis was observed in Smad3 or TGF-ß1 siRNA-transfected cells. TGF-ß1 and Smad3 mRNA and protein expression increased following TGF-ß1 and Smad3 transfection. Taken together, our experimental results show that Smad3 and TGF-ß1 play a protective role against ischemic stroke, as demonstrated by the reduced infarct size. Smad3 and TGF-ß1 expression was increased in cells transfected with TGF-ß1, whereas Smad3 and TGF-ß1 expression was increased in TGF-ß1 inhibitor-transfected cells.